"Then, when you look at the Turkey virus—that thing mutated. This is the case of the young girl in Turkey who died from her infection, and so did her uncle. We definitely have clusters where it's not just bird contact [spreading the virus]. The uncle's only exposure to this virus was riding in the ambulance with her from hospital one to hospital two. He became ill three days later and died. Her virus has now been fully sequenced, and there were three mutations that occurred in that virus, between the bird version and hers. One was the substitution of a glutamic acid with lysine at the 223-hemagglutinin position. That is what changes it from a bird-receptor virus to a human-receptor virus. The second thing was two other substitutions that served to make it look more and more like a human virus."
If that isn't human to human then what the hell is?
"Well, that's not really true. There's no evidence that it makes a difference in H5N1 infection. I have a slide here showing that the case mortality rate in Vietnam was identical for those who got Tamiflu and those who didn't. I actually believe Tamiflu could work, but the problem is, we're applying it in the H3N2 [average seasonal flu] model. Seasonal flu grows up much slower in a human, so that if you get the drug into somebody two days after their onset, you can still have a pretty measurable impact on the severity of their illness and the likelihood they'll have complications. With the H5N1 virus, the virus storm that precedes the cytokine storm is so remarkable in those first 24 hours that if you don't have the drug onboard in those first 24 hours, it may only have limited impact. The second thing is, we're using the same dosage levels we use for H3N2 [seasonal flu]. This is a very different virus. We may have to double the dosage for twice the length of time. We have anecdotal data on people who got the drug early and appeared to do better, but then, after the typical five-day course was stopped, they died on day ten."
It seems that Tamiflu only delays the inevitable.
If that isn't human to human then what the hell is?
"Well, that's not really true. There's no evidence that it makes a difference in H5N1 infection. I have a slide here showing that the case mortality rate in Vietnam was identical for those who got Tamiflu and those who didn't. I actually believe Tamiflu could work, but the problem is, we're applying it in the H3N2 [average seasonal flu] model. Seasonal flu grows up much slower in a human, so that if you get the drug into somebody two days after their onset, you can still have a pretty measurable impact on the severity of their illness and the likelihood they'll have complications. With the H5N1 virus, the virus storm that precedes the cytokine storm is so remarkable in those first 24 hours that if you don't have the drug onboard in those first 24 hours, it may only have limited impact. The second thing is, we're using the same dosage levels we use for H3N2 [seasonal flu]. This is a very different virus. We may have to double the dosage for twice the length of time. We have anecdotal data on people who got the drug early and appeared to do better, but then, after the typical five-day course was stopped, they died on day ten."
It seems that Tamiflu only delays the inevitable.
